● pain threshold is met 🠆 a stimulus is inflicted

and pain is felt but no pain complaint.

○ if a stimulus is inflicted then pain is felt
- Unpleasant sensory and emotional experience and the pt complains of pain, the pain is
associated with actual or potential tissue damage or more than the pain threshold of the
described in terms of such damage. (Association of pt.
the Study of Pain) ○ Threshold 🠆 pain na kayang tiisin ng pt
➔ causes discomfort for the client
➔ in perception of pain, it is brought about by
PAIN TOLERANCE
the sensory system.
- Time/intensity of pain endured before initiation of
◆ The human body’s sensory perception
over pain response and patient complaint.
is perceiving the cause of pain.
➔ increases d/t:
➔ the causes of pain can be physiological or
◆ alcohol consumption
psychological and emotional alterations.
◆ medication (pain meds)
◆ tissue damage (trauma, injury, or
◆ hypnosis
inflammation that the client
◆ warmth (h/c compress)
experiences)
◆ distraction
- Generally SUBJECTIVE but it can also be OBJECTIVE
➔ decreases d/t:
through pain assessment of a nurse.
◆ repeated exposure
- Can be gathered by self-report
◆ fatigue
❖ if a client doesn’t report pain, the nurse must
◆ anger
be the one to ask.
◆ apprehension
➢ “Is there discomfort?”
◆ sleep deprivation
➢ “Is there pain you experience as of the
- From the moment that there is stimulus up until the
moment?”
occurrence of pain complaints.
❖ pts who are comatose or who have dementia;
❖ since a stimulus is painful for Syra, the pain
who are mentally disabled/challenged, and
threshold (naramdaman ung sakit) and pain
pts w/ expressive aphasia have varying
tolerance is met (nagcomplain na masakit).
abilities to report pain.
❖ since a stimulus is not painful for Denice,
➢ include nonverbal infos e.g. observed
although the pain threshold is met
behaviors into your pain assessment.
(nararamdaman na may nakadagan na pencil),
the pain tolerance is not met (hindi
PAIN THRESHOLD nagcomplain na masakit).
- Point/amount at which a stimulus needed to perceive ➢ tolerance is met 🠆 the pain cannot be
pain. tolerated anymore by the pt.
➔ comes from the degree and depth of stimulus
being inflicted from the client
PAIN MECHANISM
◆ kapag kinurot ka, bakit naramdaman
Nociception
mo?
● a process where tissue damage is communicated to
◆ kapag hinawakan ung buhok mo, bakit
the CNS.
hindi mo maramdaman?
Nociceptors
◆ varying from person to person, form of
● are receptors that get and perceive pain stimuli.
uniqueness
○ Histamine
❖ degree of pain may vary from one person to
○ Bradykinin
another
○ Prostaglandin
➢ a stimulus might be painful for Syra but
○ Substance P
not for Denice (e.g.: poking w/ a pencil
○ Serotonin
with the same degree of pain)
PROCESS:
■ the pain threshold of Denice is
1. Transduction - the conversion of noxious stimuli
not the same as Syra’s.
(mechanical, thermal, chemical) into electrical signal
- From the moment that there is a stimulus up until the
(action potential).
client feels the pain.
2. Transmission - signals relayed from periphery to
● pain threshold is not met 🠆 a stimulus is
spinal cord to the brain (going to the CNS)
inflicted and no pain is felt.
Pain Physiology
 [Transduction phase starts here..]
➔ Pain perception starts with a stimulus which can be:
◆ Mechanical (when pinched or slapped)
◆ Electrical (electricity)
◆ Chemical (muriatic acid)
◆ Thermal (temperature; when too hot/cold)
➔ Once the body perceives the pain, it causes damage or injury in
the cells.
◆ The cellular injury is perceived by nociceptors so these
are activated in which it stimulates an action potential.
◆ It converts the type of energy perceived by the human
body into electrical energy through electrolyte exchange.
➔ The electrolyte exchange produces an electrical impulse.
◆ Upon production of this, there is a nerve impulse.
➔ One of the basic physiological mechanisms that the body
stimulates is the release of the inflammatory chemicals:
◆ Kinins (Bradykinin)
◆ Prostaglandin
◆ Histamine
● Through use of these two, inflammation happens
as it is the body’s primary response when there is
injury.
● These are potent vasodilators as it dilates the
blood vessels to 🠅blood flow.
○ Increased blood flow concentration in the
injured area is necessary as the cell
mediators like WBC, B cells and immune cells
in the bloodstream fights and controls the
injured area.
➔ With the occurrence of inflammation, the five cardinal signs of
inflammation appear.
◆ Calor (warmth)
◆ Rubor (redness)
◆ Tumor (swelling) 🠆 d/t fluid increase in the injured site
● 🠅Hydrostatic pressure 🠆 fluid is released into the
blood vessels 🠆 goes into interstitial spaces =
SWELL
◆ Dolor (pain) 🠆 “5th vital sign”; d/t prostaglandin release
◆ Functio Laesa (loss of function) 🠆 happens when area is
inflamed
[Transmission phase starts here…]
➔ Two types of impulses; nerve fibers:
◆ A Fibers (see table below)
◆ C Fibers (see table below)
● Both are connected to the spinal cord, entering
the dorsal horn.
○ Where also pain perception enters a.k.a 🠆
AFFERENT NERVES (from the periphery to
the brain) = AFFECT
○ EFFERENT NERVES (from brain to the
peripheral nervous system) = EFFECT
➔ From the dorsal horn, it will go up to the spinal cord up until the
thalamus of the brain.
◆ The relay center that processes the information of the
body’s senses and distributes it to the cerebral cortex
(lobe) for interpretation.
● The cortex is divided into 4 lobes: Frontal,
Temporal, Parietal, and Occipital.
○ Parietal lobe receives and interprets pain
perception.
○ Temporal lobe receives a stimulus from
the auditory nerve.
➔ When the sensation is interpreted, there is pain perception
◆ The mechanism happens in less than 1 second.
➔ ASCENDING PATHWAY OF THE NS: from transduction to
perception phase
● Perception phase happens when the brain has
already interpreted the stimulus.
◆ DESCENDING PATHWAY OF THE NS: modulation phase
i.e. when formulating a response to pain
● From the brain, goes down to thalamus 🠆 to the
spinal cord 🠆 brainstem 🠆 somatic organs (e.g.
muscles)
 CLASSIFICATION OF PAIN
Nociceptive Pain
A-delta Fibers C Fibers
- Normal processing that damages normal tissue
● w/ myelin sheath ● w/o myelin sheath (cellular or tissue damage; e.g. natapilok)
● Abrupt onset; ● SLOW impulse ➔ Somatic Nociceptive Pain
insidious transmission of pain in ◆ superficial (skin, mucous membranes
● FAST impulse the neurons & subcutaneous)
transmission in the ● ACHING/THROBBING ● SHARP, BURNING, OR PRICKLY
neurons ● CHRONIC (mabagal ◆ deep (bone, joint, muscle, skin &
● SHARP PAIN pero matagal mawala connective tissues)
● ACUTE (mabilis ang pain) ● DEEP, ACHING, THROBBING
mag-arise at mabilis ➔ Visceral Nociceptive Pain
mawala ang pain) ◆ internal organs and lining of body
cavities (thoracic, abdominal)
● Intense cramping pain when
there’s a tumor involvement
which can stretch the hollow
a. Transmission to Spinal Cord
viscera in the intestines and
b. Dorsal Horn processing
bladder.
c. Transmission to Thalamus and Cortex
◆ d/t inflammation, stretching, and
ischemia
3. Perception - pain is recognized, defined and
● E.g.: surgical incision,
assigned (conscious experience)
pancreatitis, inflammatory
bowel disease
4. Modulation - activation of descending pathways
that exert effects on pain transmission.
Neuropathic Pain
➔ Happens before the pain response goes to the
- Abnormal processing caused by damage to
periphery
peripheral nerves or structures of the CNS
➔ Using the efferent nerves 🠆 goes to spinal
● NUMBING, HOT, BURNING, SHOOTING,
cord 🠆 PNS and may be connected to muscles
STABBING, SHARP, or ELECTRIC SHOCK-LIKE
& other nerves
● Sudden, intense, short lived, or lingering
❖ Smooth muscles: involuntary
○ e.g.: trauma, inflammation, metabolic
➢ In the heart or smooth muscles
diseases (e.g. diabetes), alcoholism
surrounding the vascular
● Treatment requires a multimodal approach
system (blood vessels)
combining various adjuvant analgesics
○ When there’s pain, V/S
○ TCA (Amitriptyline)
increases
○ SNRIs (Bupropion [Wellbutrin, Zyban])
❖ Skeletal muscles: voluntary; motor
○ Antiseizure drugs (Pregabalin)
movements in response to pain
○ Transdermal Lidocaine
- Areas:
○ ⍺2-Adrenergic Agonists (Clonidine)
● periphery
● spinal cord
❖ Allodynia (pain from a normally non noxious
● brainstem; or
stimuli e.g. touch)
● cerebral cortex
➢ In pts w/ allodynia, weight of clothing or
- Chemicals:
bedsheets on skin can be excruciatingly
● serotonin
painful
● norepinephrine
● GABA (gamma-aminobutyric acid)
➔ Central Neuropathic Pain
● endogenous opioids (Endorphins,
- Primary lesion or dysfunction in CNS
Enkephalins)
● e.g.: post-stroke, multiple
○ stimulated by laughing;
sclerosis pain (CNS damage)
stimulates mood
○ SEVERE HEADACHE is the
improvement = decrease pain
primary manifestation in
stroke
➔ Peripheral Neuropathies
Acute Pain Chronic Pain
- Felt along the distribution of one or
O: Sudden O: Gradual or Sudden
many peripheral nerves d/t nerve D: <3 mos. or until healing D: >3 mos. (acute 🠆 past
damage (< 6mos) normal recovery)
● BURNING, PAROXYSMAL, or Ca: can identify a Ca: may not be known,
SHOCK-LIKE precipitating event (known) differ from other
● +/- motor & sensory signs; Co: 🠇overtime up to mechanisms
numbness, allodynia or change in recovery Co: does not go away (⭥)
reflex & motor strength S/Sx: 🠆 Intractable Pain
● e.g.: DM neuropathy, trigeminal - (+) SNS response S/Sx:
neuralgia, herpetic neuralgia [fight or flight] - Flat affect
- 🠅HR, BP. RR - 🠇Physical activity
➔ Deafferentation Pain (bronchodilation) - Fatigue
- Loss of afferent input to either - Diaphoresis - Withdrawal from
peripheral nerve injury or CNS damage (sweating) interaction
● e.g.: phantom limb, - Pallor E.g.:
postmastectomy, Spinal Cord - Anxiety ❖ Chronic gastritis
Injury - Agitation (🠅HCl acid
- Urine retention secretions)
➔ Sympathetically Maintained E.g.:
- Persistent secondary to sympathetic ❖ Musculoskeletal
activity injuries
● Dramatic changes in color & ❖ Pain from allergic
temp of skin rhinitis
● INTENSE BURNING PAIN, SKIN ❖ Post Op pain
SENSITIVITY, SWEATING, ❖ Labor pain
SWELLING ❖ Trauma (sprain,
● e.g. : phantom limb, complex fractures, lacerations)
regional pain syndrome ❖ Infection (dysuria
○ CRPS Type I triggered by: from cystitis)
tissue injury, surgery, ❖ Acute ischemia
vascular (e.g. stroke)
O-onset; D-duration; Ca-cause; Co-course; S/Sx - signs & symptom
○ CRPS Type II: peripheral
nerve lesion
CANCER-RELATED PAIN
- An 8-10/10 scale of pain that is continuously being
felt by the pt
- May or may not have physiologic signs of pain
-

THEORIES OF PAIN
Specificity Theory
● Pain is a sensory phenomenon (specific receptors,
routes of transmission - CNS, center of registration,
appreciation and interpretation of the brain)
○ Nociception

Pattern Theory
● Intensity theory
● Pain is produced by intense stimulation of
non-specific fiber receptors
● “Any stimulus could be perceived as painful if the
stimulation were intense enough”
Gate Control Theory
● Substantia gelatinosa (dorsal horn) acts as a gate ➔ Location
mechanism that can close and open to pain impulses ❖ Origin and Radiation
(the one that regulates the pain)
● (+) nerve message is pain ⟹ gate opens to the brain ➔ Intensity
● (+) conflicting impulses from on large diameter ❖ Numerical analogue scale
nerve fibers from reticular formation/thalamus ⟹ ➢ Mild: 1-3
gate closes ➢ Moderate: 4-6
● Can utilize independent pain interventions such as: ➢ Severe: 7-10
○ warm & cold compress ❖ Wong-Baker FACES Pain Scale
○ massage ➢ the facial grimace itself will identify the
○ distractions degree of pain based on the degree of
the pt’s facial grimacing
Central Control Theory
● Brain opiates (analgesic properties) release are
affected by actions initiated by the caregiver.
○ distraction therapy
○ guided imagery
○ deep breathing exercises
○ laughter & expressive therapy (art, music,
dance)

PAIN ASSESSMENT
Goal:
✔ Describe the pain experience
✔ Identify the goal for therapy and resources of ➔ Quality
self-management. ❖ Nature and characteristic
➢ e.g.: sharp, dull, throbbing, excruciating
Principles:
1. Patient right to appropriate assessment and PQRST OF PAIN
management ❖ P: Predisposing/Provoking Factors
2. Always SUBJECTIVE! ❖ Q: Quality
3. Physiologic and behavioral signs of pain are not ❖ R: Radiation
reliable or specific. ❖ S: Severity
4. Unpleasant sensory and emotional experience ❖ T: Timing
5. Assessment approaches (tools) must be
appropriate. ➔ Associated
6. Exist even when no physical cause ❖ Anxiety, fatigue, depression
7. Different experience and levels ➢ emotional states can also affect degree
8. (+) Chronic pain - may be more sensitive of pain
9. Unrelieved pain has adverse consequences
➔ Management Strategies
ELEMENTS OF PAIN ASSESSMENT ❖ Coping differences (non-pharmacologic)
➔ Pattern
❖ Pain onset ➔ Impact of Pain
❖ Duration ❖ Quality of life (sleep, enjoy life, social)
❖ Breakthrough Pain (BTP) - transient pain
even with RTC medication ➔ Belief, Expectations & Goals
➢ Tramadol 50mg TIV Q6H (6-12-6-12) ❖ Promote or hinder management
➢ Paracetamol 300mg TIV PRN x BTP
(2:30pm)
❖ Incident Pain - transient pain caused by
specific activity
 ➔ Documentation of findings and must be complete ◆ E.g.: Paracetamol 🠆 do not 🠅recommended
➔ Reassessment whether or not interventions are dosage = Hepatotoxicity
working and to see if goals are achieved ◆ Ⓧ antiplatelet/anti inflammatory
❖ Paracetamol 🠆 consider the peak time ◆ Can control pain & reduce fever 🠆 prevents
➢ Tab: 2hrs prostaglandin formation in the CNS
➢ IV: 30 mins - 1 hour
➔ Salicylates: 🠅GI bleeding
NURSING IMPLICATIONS ◆ Take it w/ FOOD to 🠇GI irritation to prevent
✔ Assess pain in all patients GI bleeding
✔ Self-report is the single most indicator ◆ e.g.: Aspirin
✔ Do not rely primarily on observance and objective ➔ NSAIDS: COX-1 🠆 protective functions (it is
signs involved sometimes in the HCL production in GI
✔ Address both physical & psychologic aspect tract)
✔ Special considerations in communication problems ◆ e.g.: Mefenamic, Ibuprofen,
✔ Include family members (when appropriate) Alaxan, Diclofenac K, Etoricoxib
✔ No uniform pain threshold (take w/ meals)
✔ Pain tolerance varies COX-2 🠆 produced in site of injury
✔ Encourage patient to report pain (produced by cells itself)
◆ e.g.: Celecoxib (safe to take w/o
PRINCIPLES OF PAIN TREATMENT (see page 3) meals; no GI upset)
1. Follow the principles in pain assessment
2. Use a holistic approach (physiol & psych) Opioids
3. Every patient deserves adequate management - Moderate to severe pain
4. Base treatment plan on patient’s goal - Binds to CNS receptors
5. Use both drug and nondrug therapies (adjunctive ● Ⓧ nociceptive input from periphery to
therapies) spinal cord
6. Use a multimodal approach to analgesic therapy ● Alter limbic system activity
(when appropriate) ● Activate descending inhibitory pathway
7. Use a multidisciplinary approach ○ Tramadol 🠆 not for ppl w/ HEADACHE
8. Evaluate the effectiveness of all therapies (proper as it is also its SIDE EFFECT
reassessment) ○ Fentanyl, Morphine, Codeine,
9. Prevent or manage medication side effects Meperidine (Demerol)
10. Patient and caregiver teaching
Opioid Agonists
PHARMACOLOGIC THERAPY - Bind to mu receptors
Non-Opioids - Acute and chronic pain
- Mild to moderate pain ● Ⓧ analgesic ceiling
- Used in conjunction with opioids (opioid-sparing ● e.g: morphine, oxycodone, codeine,
effect) methadone, oxymorphone, levorphanol, and
● Analgesic ceiling 🠆 there is degree of tramadol
effect/maximum dose
○ Paracetamol: given q4hr or q6hr Mixed Agonist-Antagonists
■ 12-4-8-12-4-8 (6 tabs can - Agonist on kappa receptors
take in 24 hrs) - Weak antagonists on mu receptors
■ If increase the dosage or ● ↓respiratory depression
frequency, destroy the liver = ● (+) analgesic ceiling, respi depressant
HEPATOTOXIC (though the ● e.g.: nalbuphine, pentazocine, butorphanol
effect is still the same d/t the (given in cancer pain or given as a sedative
analgesic ceiling) during preop meds)
● Ⓧ tolerance/dependence ○ MONITOR RR of client
● OTC (no need for prescriptions) ○ Provide mech vent

➔ Acetaminophen: analgesic + antipyretic

 Neuroaugmentation
- Electrical stimulation of the brain/spinal cord (e.g.:
TENS)
● e.g.: chronic back pain

NON DRUG THERAPIES

Physical Pain Relief Strategies
- Massage
- Exercise (releases endo opioids i.e. enkephalins &
endorphins)
- Acupuncture
- Heat and Cold therapy
- Transcutaneous Electrical nerve stimulation (TENS)

Cognitive Therapies
- Distraction
- Hypnosis
- Relaxation strategies
- Relaxation breathing
- Imagery
- Meditation
- Art and music therapy

Level 1: Opioids + adjuvant therapies

Level 2: Opioids + non-opioids
Level 3: Opioids + non-opioids

Adjuvant Therapies
- Corticosteroids (Dexamethasone, Prednisone,
Hydrocortisone, Methylprednisolone)
- Antidepressants (TCA, MAOI, SSRI)
- Antiseizure drugs (Phenytoin, Phenobarbital)
- GABA receptor antagonists (promotes release of
GABA; anxiolytics [minor tranquilizers] i.e. Valium,
Diazepam)
- Alpha-Adrenergic agonist (increases action of SNS;
stimulants; supported by coughing; Salbutamol)
- Local anesthetics (MLA, Lidocaine)
- Cannabinoids [cannabis (marijuana)]

INTERVENTIONAL THERAPY
Therapeutic Nerve Blocks
- Infusion of local anesthetics to a particular area
(regional anesthesia injected in skin)
- Local infiltration or nerve injection (parenteral)

Neuroablative Technique
- Severe pain unresponsive to other therapies
- Destroy nerves by surgical resection,
thermocoagulation, or radiofrequency
● e.g.: sensory nerve (rhizotomies), spinal cord
(cardotomies), medulla (tractotomies)